Chronic renal failure

Chronic renal failure is usually the end result of a gradually progressive loss of renal function; occasionally, it’s the result of a rapidly progressive disease of sudden onset. Few symptoms develop until after more than 75% of glomerular filtration is lost; then the remaining normal parenchyma deteriorates progressively, and symptoms worsen as renal function decreases.

If this condition continues unchecked, uremic toxins accumulate and produce potentially fatal physiologic changes in all major organ systems. If the patient can tolerate it, maintenance dialysis or kidney transplantation can sustain life.

Causes and incidence

Diabetes and hypertension are the primary causes of chronic renal failure, accounting for two-thirds of cases. Other causes of chronic renal failure include:

❑ chronic glomerular disease such as glomerulonephritis

❑ chronic infections, such as chronic pyelonephritis or tuberculosis

❑ congenital anomalies such as polycystic kidneys

❑ vascular diseases such as renal nephrosclerosis

❑ obstructive processes such as calculi

❑ collagen diseases such as systemic lupus erythematosus

❑ nephrotoxic agents such as long-term aminoglycoside therapy.

These conditions gradually destroy the nephrons and eventually cause irreversible renal failure. Similarly, acute renal failure that fails to respond to treatment becomes chronic renal failure.

This syndrome may progress through the following stages:

❑ reduced renal reserve (creatinine clearance glomerular filtration rate [GFR] is 40 to 70 ml/minute)

❑ renal insufficiency (GFR 20 to 40 ml/ minute)

❑ renal failure (GFR 10 to 20 ml/minute)

❑ end-stage renal disease (GFR less than 10 ml/minute).

Chronic renal failure and end-stage renal disease affect about 2 out of 1,000 people in the United States.

Signs and symptoms

Chronic renal failure produces major changes in all body systems:

❑ Renal and urologic: Initially, salt-wasting and consequent hyponatremia produce hypotension, dry mouth, loss of skin turgor, listlessness, fatigue, and nausea; later, somnolence and confusion develop. As the number of functioning nephrons decreases, so does the kidneys’capacity to excrete sodium, resulting in salt retention and overload. Accumulation of potassium causes muscle irritability, then muscle weakness as the potassium level continues to rise. Fluid overload and metabolic acidosis also occur. Urinary output decreases; urine is very dilute and contains casts and crystals.

❑ Cardiovascular: Renal failure leads to hypertension, arrhythmias (including life-threatening ventricular tachycardia or fibrillation), cardiomyopathy, uremic pericarditis, pericardial effusion with possible cardiac tamponade, heart failure, and periorbital and peripheral edema.

❑ Respiratory: Pulmonary changes include reduced pulmonary macrophage activity with increased susceptibility to infection, pulmonary edema, pleuritic pain, pleural friction rub and effusions, crackles, thick sputum, uremic pleuritis and uremic lung (or uremic pneumonitis), dyspnea due to heart failure, and Kussmaul’s respirations as a result of acidosis.

❑ GI: Inflammation and ulceration of GI mucosa cause stomatitis, gum ulceration and bleeding and, possibly, parotitis, esophagitis, gastritis, duodenal ulcers, lesions on the small and large bowel, uremic colitis, pancreatitis, and proctitis. Other GI symptoms include a metallic taste in the mouth, uremic fetor (ammonia smell to breath), anorexia, nausea, and vomiting.

❑ Cutaneous: Typically, the skin is pallid, yellowish bronze, dry, and scaly. Other cutaneous symptoms include severe itching; purpura; ecchymoses; petechiae; uremic frost (most often in critically ill or terminal patients); thin, brittle fingernails with characteristic lines; and dry, brittle hair that may change color and fall out easily.

❑ Neurologic: Restless leg syndrome, one of the first signs of peripheral neuropathy, causes pain, burning, and itching in the legs and feet, which may be relieved by voluntarily shaking, moving, or rocking them. Eventually, this condition progresses to paresthesia and motor nerve dysfunction (usually bilateral footdrop) unless dialysis is initiated. Other signs and symptoms include muscle cramping and twitching, shortened memory and attention span, apathy, drowsiness, irritability, confusion, coma, and seizures. EEG changes indicate metabolic encephalopathy.

❑ Endocrine: Common endocrine abnormalities include stunted growth patterns in children (even with elevated growth hormone levels), infertility and decreased libido in both sexes, amenorrhea and cessation of menses in females, and impotence, decreased sperm production, and testicular atrophy in males. Increased aldosterone secretion (related to increased renin production) and impaired carbohydrate metabolism (increased blood glucose levels similar to diabetes mellitus) may also occur.

❑ Hematopoietic: Anemia, decreased red blood cell (RBC) survival time, blood loss from dialysis and GI bleeding, mild thrombocytopenia, and platelet defects occur. Other problems include increased bleeding and clotting disorders, demonstrated by purpura, hemorrhage from body orifices, easy bruising, ecchymoses, and petechiae.

❑ Skeletal: Calcium-phosphorus imbalance and consequent parathyroid hormone imbalances cause muscle and bone pain, skeletal demineralization, pathologic fractures, and calcifications in the brain, eyes, gums, joints, myocardium, and blood vessels. Arterial calcification may produce coronary artery disease. In children, renal osteodystrophy (renal rickets) may develop.

Diagnosis

Diagnosis of chronic renal failure is based on clinical assessment, a history of chronic progressive debilitation, and gradual deterioration of renal function as determined by creatinine clearance tests. The following laboratory findings also aid in diagnosis:

❑ Blood studies show elevated blood urea nitrogen, serum creatinine, and potassium levels; decreased arterial pH and bicarbonate; and low hemoglobin (Hb) level and hematocrit (HCT).

❑ Urine specific gravity becomes fixed at 1.010; urinalysis may show proteinuria, glycosuria, erythrocytes, leukocytes, and casts, depending on the etiology.

❑ X-ray studies include kidney-ureter-bladder films, excretory urography, nephrotomography, renal scan, and renal arteriography.

❑ Renal or abdominal computed tomography scan, magnetic resonance imaging, or ultrasound indicate changes associated with chronic renal failure, including abnormally small size in both kidneys.

❑ Kidney biopsy allows histologic identification of the underlying pathology.

Treatment

Treatment focuses on controlling the symptoms, minimizing complications, and slowing the progression of the disease. Associated diseases that cause or result from chronic renal failure must be controlled such as hypertension. Conservative treatment aims to correct specific symptoms. A low-protein diet reduces the production of end products of protein metabolism that the kidneys can’t excrete. (A patient receiving continuous peritoneal dialysis should have a high-protein diet.) A high-calorie diet prevents ketoacidosis and the negative nitrogen balance that results in catabolism and tissue atrophy, and restricts sodium and potassium.

Maintaining fluid balance requires careful monitoring of vital signs, weight changes, and urine volume (if present). If some renal function remains, administration of loop diuretics such as furosemide, and fluid restriction can reduce fluid retention. Cardiac glycosides may be used to mobilize edema fluids; antihypertensives, to control blood pressure and associated edema. Antiemetics taken before meals may relieve nausea and vomiting; cimetidine or ranitidine may decrease gastric irritation. Methylcellulose or docusate can help prevent constipation.

Treatment may also include regular stool analysis (guaiac test) to detect occult blood and, as needed, cleaning enemas to remove blood from the GI tract. Anemia necessitates iron and folate supplements; severe anemia requires infusion of fresh frozen packed cells or washed packed cells. However, transfusions relieve anemia only temporarily. Epoetin alpha (erythropoietin) increases RBC production.

Drug therapy often relieves associated symptoms: an antipruritic, such as trimeprazine or diphenhydramine, for itching and aluminum hydroxide gel to lower serum phosphate levels. The patient may also benefit from supplementary vitamins (particularly B vitamins and vitamin D) and essential amino acids.

Careful monitoring of serum potassium levels is necessary to detect hyperkalemia. Emergency treatment for severe hyperkalemia includes dialysis therapy and administration of 50% hypertonic glucose I.V., regular insulin, calcium gluconate I.V., sodium bicarbonate I.V., and cation exchange resins such as sodium polystyrene sulfonate.

Alert Cardiac tamponade resulting from pericardial effusion may require emergency pericardial tap or surgery.

Blood gas measurements may indicate acidosis; intensive dialysis and thoracentesis can relieve pulmonary edema and pleural effusions.

Hemodialysis or peritoneal dialysis (particularly continuous ambulatory peritoneal dialysis and continuous cyclic peritoneal dialysis) can help control most manifestations of end-stage renal disease; altering dialyzing bath fluids can correct fluid and electrolyte disturbances. (See Comparing peritoneal dialysis and hemodialysis, page 806. Also see Continuous ambulatory peritoneal dialysis, page 807.) But anemia, peripheral neuropathy, cardiopulmonary and GI complications, sexual dysfunction, and skeletal defects may persist. Maintenance dialysis itself may produce complications, such as protein wasting, refractory ascites, and dialysis dementia. Kidney transplantation may eventually be the treatment of choice for some patients with end-stage renal disease.

PEDIATRIC TIP Children require more dialysis in relation to their body weight than adults because their metabolic rates and, therefore, food intake, are higher.

Special considerations

Because chronic renal failure has such widespread clinical effects, it requires meticulous and carefully coordinated supportive care.

❑ Good skin care is important. Bathe the patient daily, using superfatted soaps, oatmeal baths, and skin lotion without alcohol to ease pruritus. Don’t use glycerin-containing soaps because they’ll cause skin drying. Give good perineal care, using mild soap and water. Pad the side rails to guard against ecchymoses. Turn the patient often, and use a convoluted foam mattress to prevent skin breakdown.

❑ Provide good oral hygiene. Brush the patient’s teeth often with a soft brush or sponge tip to reduce breath odor. Sugarless hard candy and mouthwash minimize bad taste in the mouth and alleviate thirst.

❑ Offer small, palatable meals that are also nutritious; try to provide favorite foods within dietary restrictions. Encourage intake of high-calorie foods. Instruct the outpatient to avoid high-sodium foods and high-potassium foods. Encourage adherence to fluid and protein restrictions. To prevent constipation, stress the need for exercise and sufficient dietary bulk.

❑ Watch for hyperkalemia. Observe for cramping of the legs and abdomen, and diarrhea. As potassium levels rise, watch for muscle irritability and a weak pulse rate. Monitor the electrocardiogram for tall, peaked T waves, widening QRS segment, prolonged PR interval, and disappearance of P waves, indicating hyperkalemia.

❑ Assess hydration status carefully. Check for jugular vein distention, and auscultate the lungs for crackles. Measure daily intake and output carefully, including all drainage, emesis, diarrhea, and blood loss. Record daily weight, presence or absence of thirst, axillary sweat, dryness of tongue, hypertension, and peripheral edema.

❑ Monitor for bone or joint complications. Prevent pathologic fractures by turning the patient carefully and ensuring his safety. Provide passive range-of-motion exercises for the bedridden patient.

❑ Encourage deep breathing and coughing to prevent pulmonary congestion. Listen often for crackles, rhonchi, and decreased breath sounds. Be alert for clinical effects of pulmonary edema (dyspnea, restlessness, crackles). Administer diuretics and other medications, as ordered.

❑ Maintain strict sterile technique. Use a micropore filter during I.V. therapy. Watch for signs of infection (listlessness, high fever, and leukocytosis). Urge the outpatient to avoid contact with infected persons during the cold and flu season.

❑ Carefully observe and document seizure activity. Infuse sodium bicarbonate for acidosis, and sedatives or anticonvulsants for seizures, as ordered. Pad the side rails and keep an oral airway and suction setup at bedside. Assess neurologic status periodically, and check for Chvostek’s and Trousseau’s signs, indicators of low serum calcium levels.

❑ Observe for signs of bleeding. Watch for prolonged bleeding at puncture sites and at the vascular access site used for hemodialysis. Monitor Hb levels and HCT, and check stool, urine, and vomitus for blood.

❑ Report signs of pericarditis, such as a pericardial friction rub and chest pain.

Alert Watch for the disappearance of friction rub, with a drop of 15 to 20 mm Hg in blood pressure during inspiration (paradoxical pulse) — an early sign of pericardial tamponade.

❑ Schedule medications carefully. Give iron before meals, aluminum hydroxide gels after meals, and antiemetics, as necessary, a half hour before meals. Administer antihypertensives at appropriate intervals. If the patient requires a rectal infusion of sodium polystyrene sulfonate for dangerously high potassium levels, apply an emollient to soothe the perianal area. Be sure the sodium polystyrene sulfonate enema is expelled; otherwise, it will cause constipation and won’t lower potassium levels. Recommend antacid cookies as an alternative to aluminum hydroxide gels needed to bind GI phosphate.

If the patient requires dialysis:

❑ Prepare the patient by fully explaining the procedure. Be sure that he understands how to protect and care for the arteriovenous shunt, fistula, or other vascular access. Check the vascular access site per facility protocol or every 2 hours for patency and the extremity for adequate blood supply and intact nervous function (temperature, pulse rate, capillary refill, and sensation). If a fistula is present, feel for a thrill and listen for a bruit. Use a gentle touch to avoid occluding the fistula. Report signs of possible clotting. Don’t use the arm with the vascular access site to take blood pressure readings, draw blood, or give injections as these procedures may rupture the fistula or occlude blood flow.

❑ Withhold the 6 a.m. (or morning) dose of antihypertensive on the morning of dialysis, and instruct the outpatient to do the same.

❑ Use standard precautions when handling body fluids and needles.

❑ Monitor Hb levels and HCT. Assess the patient’s tolerance of his levels. Some individuals are more sensitive to lower levels than others. Instruct the anemic patient to conserve energy and to rest frequently.

❑ After dialysis, check for disequilibrium syndrome, a result of sudden correction of blood chemistry abnormalities. Symptoms range from a headache to seizures. Also, check for excessive bleeding from the dialysis site. Apply pressure dressing or absorbable gelatin sponge, as indicated. Monitor blood pressure carefully after dialysis.

❑ A patient undergoing dialysis is under a great deal of stress, as is his family. Refer them to appropriate counseling agencies for assistance in coping with chronic renal failure.

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Book Source Details

• Book Title: Professional Guide to Diseases (Eighth Edition)
• Author(s): Springhouse
• Year of Publication: 2005
• Copyright Details: Professional Guide to Diseases (Eighth Edition), Copyright © 2005 Lippincott Williams & Wilkins.

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